{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T20:02:05Z","timestamp":1760299325584,"version":"build-2065373602"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,3,10]],"date-time":"2016-03-10T00:00:00Z","timestamp":1457568000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2016,4]]},"abstract":"<jats:p>The calcium channel blocker (CCB), nifedipine, is a more effective treatment for early\u2010 than late\u2010stage cardiac hypertrophy. We investigated the effects of early\u2010 and late\u2010stage nifedipine administration on calcium homeostasis, CaMKII (Ca<jats:sup>2+<\/jats:sup>\/calmodulin\u2010dependent protein kinase II) activity and apoptosis of cardiomyocytes under hypertrophic stimulation with angiotensin II (AngII). Primary rat cardiomyocytes were divided into five treatment groups: AK, AngII plus the CaMKII inhibitor, KN\u201093; AN\u20101 (early\u2010stage), AngII plus nifedipine\u2009\u00d7\u200948\u2009h; AN\u20102 (late\u2010stage), AngII\u2009\u00d7\u200948\u2009h, then AngII plus nifedipine\u2009\u00d7\u200948\u2009h; C, untreated; and A, AngII\u2009\u00d7\u200948\u2009h. The t1\/2\u03b2 [time required for intracellular Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]i) to decline to one half of the peak value] decreased; however, CaMKII and SERCA2a (sarcoplasmic reticulum Ca<jats:sup>2+<\/jats:sup>\u2010ATPase 2a) activities increased in the AN\u20101 group compared with the AK group. In the AN\u20102 group compared with the AN\u20101 group, CaMKII activity, t1\/2\u03b1 [time required for [Ca<jats:sup>2+<\/jats:sup>]i to increase from the bottom to one half of peak value], t1\/2\u03b2, and apoptosis increased. These results indicate that the timing of CCB administration affects the calcium concentration and apoptosis of hypertrophic cardiomyocytes through the CaMKII\u2013SERCA2a signalling pathway, thereby influencing the drug's protective activity against cardiomyocyte hypertrophy. 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